Monday, November 28, 2016

A recent report in the journal Science proposed a big change in how we understand the sympathetic and parasympathetic pathways of the autonomic nervous system (ANS).

In a nutshell, the new model stipulates that the outflow (efferent pathways) are divided into a cranial division and spinal division—not the craniosacral and thoracolumbar divisions that we learned (and that exist in all A&P textbooks):Current model:

Craniosacral division (parasympathetic outflow)

Thoracolumbar division (sympathetic outflow)

New model:

Cranial division (parasympathetic outflow)

Spinal division (sympathetic outflow)

The authors lay out embryological and genetic phenotype evidence to show that the sacral components of the ANS outflow pathways are similar to sympathetic thoracic pathways—not to cranial parasympathetic pathways as we have long supposed.

But wait, you say, what about the parasympathetic control of the genitals, rectum, bladder? What about, well, all kinds of things that now seem to unravel? I suggest reading the rather brief and plainly written article in Science for the full answer.

However, a few quick points may reduce your blood pressure a bit—and perhaps pique your interest.

Quick points about the new ANS model

Thoracic and sacral pathways share common embryologic development by location and when looking at transcriptional markers associated with neurotransmitters that differ from the developmental pattern of cranial pathways.

Thoracic and sacral pathways have a ventral exit point from the spinal cord; cranial pathways have a dorsal exit point.

The pelvic ganglion has been considered a "mixed" sympathetic/parasympathetic ganglion because it receives fibers from both the upper lumbar and sacral segments. But if the sacral pathways are sympathetic, the pelvic ganglion is clearly a sympathetic ganglion (not mixed).

Analyses of transcription factors show that cells of the pelvic ganglia resemble those sympathetic ganglia and do not resemble cells in cranial ganglia.

The supposed lumbar vs. sacral antagonism in the urinary bladder's detrusor muscle does not seem to hold up, with the lumbar inhibitory effects either not demonstrable in experiments or of questionable functional relevance.

The effects on vessel dilation in genitals can be explained as a "continuity of action—rather than antagonism"

The sacral pathway to the rectum seems to resemble sympathetic structure, not cranial (parasympathetic) structure.

What can we use from this in teaching undergraduate A&P?

Consider using this scenario to illustrate the dynamic nature of science. Perhaps discuss that long-held dogma is occasionally challenged using newer methods and ways of thinking.

Consider discussing pros and cons of adopting the new model. For example, can evidence from mice extend to all vertebrates? Which is stronger, evidence for the current model or the new model? Which model is most useful in understanding principles of ANS regulation? A little critical thinking never hurt anyone (at least not much).

Companion article to the report cited above, stating that "This finding provokes a serious shift in textbook knowledge, and, as with any fundamental discovery, it brings important practical implications..." and goes on to mention of a few of the implications (e.g., how to treat bladder dysfunction).

Wednesday, November 16, 2016

Ever been part of a conversation among faculty about "students these days" and how unmotivated they are, or how they lack the skills or knowledge that you'd like them to have? Yeah, me too.

Today in my dailyNuzzel newsletter, I shared an excellent article fromFaculty Focus that does a great job of exposing the dangers of such conversations. Dangers to students, dangers to our academic institutions, and dangers to ourselves as educators. Although the author, Maryellen Wiemer, admits that occasional venting to a trusted colleagues helps us put things in perspective, she also points out the many harms that outright chronic complaining can do.

I'm not going to summarize that article here—it's best read in it's entirety. However, I'd like to add my two cents. After all, what's the good of having my own blog if I can't do that once in a while, eh?

It took me decades of teaching in high school and college classrooms to fully realize what I think my role as an A&P professor should be. It's not solely to guide well-prepared, self-motivated, highly skilled students to the success that they can easily achieve without me. Sure, that's easy and mostly annoyance-free. But it can be awfully boring. What do they need me for, anyway? Not much.

I came to discover that what really rocks my boat as a professor is when I can help a struggling student achieve even a very small success. When I can help a learning-disabled student find ways to "get it" when studying those messy histology specimens. When I can help under-prepared students "catch up" and learn some effective study skills to continue keeping up. When I can get through to unfocused, unmotivated, immature students in some small way.

We pay a lot of lip service to making our courses "student centered" and making carefully devised learning outcomes our primary goal, but we often just don't want to do the work—or put up with the frustrations—of really making that happen.

It's when I finally started embracing those challenges and leaving aside my unhelpful judgments of "students these days" that I finally started truly and totally loving teaching my A&P students. I found that the more I connected with "problem students," the closer I got to finding the underlying reasons for their apparent lack of will or ability—and thus able to help them find appropriate strategies to succeed.

Sometimes, sporadic attendance is more about serious family or health issues than it is about their attitude toward my course. Sometimes, their lack of focus in my class is more about neurological issues, personal emergencies outside the classroom, or side effects of an illness or therapy, than it is about them "not caring" about their learning. Sometimes, their lack of reading is more about dyslexia than it is about laziness.

Sure, it's sometimes hard to face challenges. Otherwise, we wouldn't call them challenges, eh? But when I ask myself, "what kind of teacher do I want to be today?" the answer always comes back to, "the kind who is going to help even the most challenging students." And that makes all the difference.

Monday, October 31, 2016

We are only very slowly recognizing the many biological and medical differences between males and females (and masculine/feminine)—besides the obvious ones related to reproduction. There are divergent patterns in the anatomy and physiology of perhaps every body system. However, in medical research male and female subjects are often grouped together in a way that obscures those divergent patterns.

Two "viewpoint" articles in the Journal of the American Medical Association (JAMA) today focus a light on this issue and point the way to improved—more clinically useful—medical research. Links to both articles are listed below.

As one of the articles points out, women have been included in medical trials for only the past few decades. So there is still a lot of work to be done to shore up the database of male-female differences. But also a lot of work to be done in sorting out male-female patterns of health and disease. Then even more work in making this new knowledge part of the everyday practice medicine.

Both articles are brief and relatively nontechnical, but when read together, they provide an important message for those of us teaching pre-clinical health professionals in A&P. That message is that we should consider introducing—then reinforcing—the notion of body-wide sex and gender differences.

Both articles give examples of such differences, but many more are to be found elsewhere, as well. Not that we should teach every possible example in the undergraduate A&P course. However, the general concept of functional variation between males and females may be an important one to emphasize as a sub-theme in our story of the human body.

What can we use from this in teaching undergraduate A&P?

Consider making sex differences a sub-theme in your A&P course.

Occasionally point out examples of structural, functional, and clinical patterns of variation that differ between males and females.

Compare and contrast sex differences with other types of pattern variations.

Discuss "patterns of variability" in contrast to a strictly "binary" view.

Consider bringing up sex-difference research that is not yet fully supported.

Discuss whether more attention to sex differences across topics in scientific research might help advance this area of knowledge.

Discuss the opposing view that there are no clinically significant biological differences between males and females other than those related to reproduction.

Look for such examples in your textbook and other teaching/learning resources and point them out to your students.

Consider having a classroom or online discussion of this topic.

Ask students to post links to articles that discuss male-female patterns of variation

Post to course discussion or course social media channel

Bring to class or email to instructor to share with class

Post on bulletin board

Bring up this issue when discussing how science is done.

Consider asking students what effects on public health a more thorough consideration of sex differences may produce.

Ask students to look at a study and ask whether sex differences were thoroughly accounted for in the methodology. Could this affect how the study is interpreted and applied in the clinic?

Want to know more?

Consideration of Sex Differences in Medicine to Improve Health Care and Patient Outcomes

This concept emerged during the 1960's, when researchers first observed that the cell could destroy its own contents by enclosing it in membranes, forming sack-like vesicles that were transported to a recycling compartment, called the lysosome, for degradation.

Difficulties in studying the phenomenon meant that little was known until, in a series of brilliant experiments in the early 1990's, Yoshinori Ohsumi used baker's yeast to identify genes essential for autophagy. He then went on to elucidate the underlying mechanisms for autophagy in yeast and showed that similar sophisticated machinery is used in our cells.

Ohsumi's discoveries led to a new paradigm in our understanding of how the cell recycles its content. His discoveries opened the path to understanding the fundamental importance of autophagy in many physiological processes, such as in the adaptation to starvation or response to infection. Mutations in autophagy genes can cause disease, and the autophagic process is involved in several conditions including cancer and neurological disease.

Degradation – a central function in all living cells

In the mid 1950's scientists observed a new specialized cellular compartment, called an organelle, containing enzymes that digest proteins, carbohydrates and lipids. This specialized compartment is referred to as a "lysosome" and functions as a workstation for degradation of cellular constituents. The Belgian scientist Christian de Duve was awarded the Nobel Prize in Physiology or Medicine in 1974 for the discovery of the lysosome.

New observations during the 1960's showed that large amounts of cellular content, and even whole organelles, could sometimes be found inside lysosomes. The cell therefore appeared to have a strategy for delivering large cargo to the lysosome. Further biochemical and microscopic analysis revealed a new type of vesicle transporting cellular cargo to the lysosome for degradation (Figure 1).

Christian de Duve, the scientist behind the discovery of the lysosome, coined the term autophagy, "self-eating", to describe this process. The new vesicles were named autophagosomes.

Figure 1: Autophagosome. Our cells have different specialized compartments. Lysosomes constitute one such compartment and contain enzymes for digestion of cellular contents. A new type of vesicle called autophagosome was observed within the cell. As the autophagosome forms, it engulfs cellular contents, such as damaged proteins and organelles. Finally, it fuses with the lysosome, where the contents are degraded into smaller constituents. This process provides the cell with nutrients and building blocks for renewal.

During the 1970's and 1980's researchers focused on elucidating another system used to degrade proteins, namely the "proteasome". Within this research field Aaron Ciechanover, Avram Hershko and Irwin Rose were awarded the 2004 Nobel Prize in Chemistry for "the discovery of ubiquitin-mediated protein degradation". The proteasome efficiently degrades proteins one-by-one, but this mechanism did not explain how the cell got rid of larger protein complexes and worn-out organelles. Could the process of autophagy be the answer and, if so, what were the mechanisms?

A groundbreaking experiment

Yoshinori Ohsumi had been active in various research areas, but upon starting his own lab in 1988, he focused his efforts on protein degradation in the vacuole, an organelle that corresponds to the lysosome in human cells.

Yeast cells are relatively easy to study and consequently they are often used as a model for human cells. They are particularly useful for the identification of genes that are important in complex cellular pathways. But Ohsumi faced a major challenge; yeast cells are small and their inner structures are not easily distinguished under the microscope and thus he was uncertain whether autophagy even existed in this organism.

Ohsumi reasoned that if he could disrupt the degradation process in the vacuole while the process of autophagy was active, then autophagosomes should accumulate within the vacuole and become visible under the microscope. He therefore cultured mutated yeast lacking vacuolar degradation enzymes and simultaneously stimulated autophagy by starving the cells.

The results were striking! Within hours, the vacuoles were filled with small vesicles that had not been degraded (Figure 2). The vesicles were autophagosomes and Ohsumi's experiment proved that authophagy exists in yeast cells. But even more importantly, he now had a method to identify and characterize key genes involved this process. This was a major break-through and Ohsumi published the results in 1992.

Figure 2: Yeast. In yeast (left panel) a large compartment called the vacuole corresponds to the lysosome in mammalian cells. Ohsumi generated yeast lacking vacuolar degradation enzymes. When these yeast cells were starved, autophagosomes rapidly accumulated in the vacuole (middle panel). His experiment demonstrated that autophagy exists in yeast. As a next step, Ohsumi studied thousands of yeast mutants (right panel) and identified 15 genes that are essential for autophagy.

Autophagy genes are discovered

Ohsumi now took advantage of his engineered yeast strains in which autophagosomes accumulated during starvation. This accumulation should not occur if genes important for autophagy were inactivated. Ohsumi exposed the yeast cells to a chemical that randomly introduced mutations in many genes, and then he induced autophagy.

His strategy worked! Within a year of his discovery of autophagy in yeast, Ohsumi had identified the first genes essential for autophagy. In his subsequent series of elegant studies, the proteins encoded by these genes were functionally characterized. The results showed that autophagy is controlled by a cascade of proteins and protein complexes, each regulating a distinct stage of autophagosome initiation and formation (Figure 3).

Figure 3: Stages of autophagosome formation. Ohsumi studied the function of the proteins encoded by key autophagy genes. He delineated how stress signals initiate autophagy and the mechanism by which proteins and protein complexes promote distinct stages of autophagosome formation.

Autophagy – an essential mechanism in our cells

After the identification of the machinery for autophagy in yeast, a key question remained. Was there a corresponding mechanism to control this process in other organisms? Soon it became clear that virtually identical mechanisms operate in our own cells. The research tools required to investigate the importance of autophagy in humans were now available.

Thanks to Ohsumi and others following in his footsteps, we now know that autophagy controls important physiological functions where cellular components need to be degraded and recycled.

Autophagy can rapidly provide fuel for energy and building blocks for renewal of cellular components, and is therefore essential for the cellular response to starvation and other types of stress.

After infection, autophagy can eliminate invading intracellular bacteria and viruses. Autophagy contributes to embryo development and cell differentiation. Cells also use autophagy to eliminate damaged proteins and organelles, a quality control mechanism that is critical for counteracting the negative consequences of aging.

Disrupted autophagy has been linked to Parkinson's disease, type 2 diabetes and other disorders that appear in the elderly. Mutations in autophagy genes can cause genetic disease. Disturbances in the autophagic machinery have also been linked to cancer. Intense research is now ongoing to develop drugs that can target autophagy in various diseases.

Autophagy has been known for over 50 years but its fundamental importance in physiology and medicine was only recognized after Yoshinori Ohsumi's paradigm-shifting research in the 1990's. For
Yoshinori Ohsumi was born 1945 in Fukuoka, Japan. He received a Ph.D. from University of Tokyo in 1974. After spending three years at Rockefeller University, New York, USA, he returned to the University of Tokyo where he established his research group in 1988. He is since 2009 a professor at the Tokyo Institute of Technology.

More background on the winner and the prize

Yoshinori Ohsumi was born in Fukuoka, Japan, in 1945. He is affiliated with the Tokyo Institute of Technology in Tokyo, Japan. His monetary award will be nearly one million dollars.

The Nobel Assembly, consisting of 50 professors at Karolinska Institutet, awards the Nobel Prize in Physiology or Medicine. Its Nobel Committee evaluates the nominations. Since 1901 the Nobel Prize has been awarded to scientists who have made the most important discoveries for the benefit of mankind.his discoveries, he is awarded this year's Nobel Prize in physiology or medicine.

Nobel Prize® is the registered trademark of the Nobel Foundation

What can we use from this in teaching undergraduate A&P?

Consider using the Nobel Prizes as a discussion-starter in your class about

How science influences society

How society influences science

How science progresses

Rewarding of science discoveries

What makes a discovery "important"

Relate this discovery to prior (or upcoming) discussions of

Cell function

Organelle specialization

How cells handle protein

How autophagosomes work with lysosomes

Compare/contrast with phagocytosis

Compare/contrast with proteasome function and protein "quality control

Relate this discovery to the general idea of cellular mechanisms of disease

Consider taking this opportunity to emphasize "why we need to know all this" detail about cellular structure and function.

Want to know more?

Scientific Background Discoveries of Mechanisms for Autophagy

Larsson, N-G, Msucci, M. G. Nobelprize.org accessed 8 October 2016

A more advanced summary of the prizewinning discovery, including a handy glossary of terms.

Monday, September 5, 2016

One of the most effective enhancements I've ever made to my human anatomy & physiology course was switching to cumulative testing. What I mean by that is instead of testing on each topic once, then moving on to a test on the next topic, I started testing my students on all the covered topics (thus far in the course) in each successive test.

I've always had a comprehensive exam at the end of the course—and eventually added a comprehensive midterm exam, too. I found that adding that midterm helped my students relearn what they'd forgotten during the first half of the semester—making them better prepared for the comprehensive final. But not a whole lot better.

As I got older and wiser—or at least grayer—and got more serious about seeking out solid research on how people actually learn new information and retain it for the long term, I realized that my thinking was sort of alongside the right track. But not fully on the right track. It finally dawned on me that I could not expect my students to really "get it" and "keep it" unless they were repeatedly challenged with a variety of test items that required them to dig back into their memories and drag out those "old" ideas from early in the course.

Learning experts sometimes call this retrieval practice. The students practice retrieving their stored knowledge and skills. One of the key elements of using retrieval practice in learning is that it is most effective when it is spaced out over time. That is, it occurs after the brain has had time to do some forgetting.

The "re-learning" and "re-remembering" that must happen after a spaced interval is one of the keys to getting it all solidly embedded into our memory. As my tai chi teacher always tells me, "you can't master it until you've forgotten it." The forgetting, making mistakes, and relearning also enhances our ability to get those concepts and skills back out of memory—thus enabling us to retrieve it when we need to apply it.

Of course, most of the effort in getting my course on the right track in this regard was getting over that same old, often insurmountable, hurdle of taking a step outside of the "way we've always done it." This nearly universal mindset not only holds me back from trying new things—it encourages my colleagues and students to tell me how wrong I am when I do.

After at least a year of self-doubt, I just forged ahead and tried it. Every one of my tests now includes test items from all previous topics. I told my students ahead of time why I was doing it and why. And guess what? They were okay with it! I didn't tell any of my colleagues what I was doing because, er, my internal voice was already telling me I was doing it all wrong.

And you know what? Without changing much else in my course that semester, the comprehensive exam grades—and even the course grades—went up almost a whole letter grade on average. In other words, my course activities and testing covered the same content, at the same level of rigor, but my students were apparent much more successful in their ability to recall the information and skills they need to solve problems at the end of the course.

This was about ten or so years ago, and I probably still have the numbers somewhere. I didn't do a statistical analysis and I didn't have a control group—unless you count sections of the course in previous semesters. But I didn't—and still don't—feel I really need that. My student grades that semester (and ever since) show a dramatic increase that I'm not willing to reverse.

Looking back through the lens of 20/20 hindsight, I can see that this should have been plain to me all along. How can we expect anyone to learn something deeply and for the long term, if they only get one chance to have their knowledge and skills challenged? Only through repeated challenges can we master concepts at a level of usefulness.

We expect our students to build a complete enough conceptual framework to see patterns and understand relationships among concepts. To really see the big picture. But do we give them enough practice to do that effectively? Or do we let them forget what they know and fail to give them those critical opportunities to relearn, thereby solidifying, key concepts?

In my experience, cumulative testing is a valuable strategy to enhance learning in our courses.

What can we use from this in teaching undergraduate A&P?

Adding items to every test that review all previous topics convert your testing strategy to cumulative testing. This may provide the repetitive, spaced retrieval practice that students need for learning for the long term.

Consider using a cumulative strategy for other forms of retrieval practice in your course. For example:

This is book written for the average teacher or student to help them understand what we now know about effective learning that may be different then the traditional approaches. You really need to read this book! It's well written, engaging, and has a wealth of great ideas.

Monday, August 8, 2016

A new study published in Advances in Physiology Education adds additional evidence of the effectiveness that students do better when they take the time to analyze their tests immediately after taking them.

In my blog The A&P Student, I published an article in October of 2009 that outlines an easy and effective way for A&P students to "debrief" after each test and exam so that they can both clarify misconceptions and gain insights into possible weakness in test preparation.

By having students focus on missed questions coupled with addressing deficiencies in their test preparation strategies and behaviors, they likely engage in more self-regulated learning to better prepare for exams and avoid repeating past mistakes. (Favero & Hendricks 2016).

What can we use from this in teaching undergraduate A&P?

Encouraging students to debrief after every test and exam—individually or in study groups—can be more effective than whole-class reviews of exams or tests.

Test self-analysis can help students learn (or re-learn) concepts they are unable to retrieve on a test.

Test self-analysis can help students identify patterns of misconceptions, poor test preparation, and poor test-taking skills that make them better aware of their own thinking (metacognition) and thus more likely to succeed in later testing.

Consider encouraging your students to debrief after every test by providing them with the tools needed (see the links below).

In my many years of using this technique, I've found that the process described in the links below works equally well for either/both online tests (including adaptive quizzing) and traditional paper tests and exams

Brief blog post directed at A&P students giving them resources to perform this on their own, including an instructional video (see below), and access to a sample analysis form (see below). Consider linking to this post in your syllabus (and/or the other embedded resources).

Entry from Kevin's library of Study Tips & Tools for A&P students, briefly runs through the advantages of debriefing after a test and provides an instructional video (see below) and sample analysis form that students can download and use (or adapt). Consider adding a link from your syllabus or course website/LMS.

Brief paperback book that you can make available in your school or classroom library or require/suggest for purchase in your college bookstore. Covers the process of test debriefing and gives tips on how to resolves inefficient patterns of test preparation and test taking. Also contains A&P specific content tips and analogies.

Wednesday, February 17, 2016

Every once in a while, I get an A&P student who expresses the concept of a negative Rh blood type as "having negative blood"—along with the connotation that having this blood type has a negative health impact.

We do not ordinarily think about red blood cell types such as A, B, AB, O, Rh+/-, or others, as being "bad for you" or even "good for you" healthwise. We most often think of them simply as different "flavors" of RBCs present in the human population.

Oh yeah, there are specific situations in which have a particular blood type can have significant health consequences. If you need an organ or tissue transplant—especially a blood donation—having the same RBC type as the available donor supply is "good for you." The lack thereof, then, is "bad for you" to at least some degree. Just like being tall can be bad for you when going through a low doorway.

Likewise, we all know there are health risks associated with a Rh- mother carrying an Rh+ fetus—especially the situation is not identified or if precautions are not taken. But it's not like the Rh- type itself has a direct health impact on the person with that type.

However, such a view may be a bit more complex than it first seems. Research continues to confirm that having a particular RBC type may affect your risk for certain health conditions.

For example, a little over a year ago, research published in the journal Neurology found that adults with type AB blood were at an increased risk of cognitive impairment compared to type O. Of course, much more work needs to be done to establish a potential mechanism for this phenomenon. But it does give some evidence that the idea of certain blood types having health consequences may be true.

Other studies have suggested these links:

Type O may be linked to depression, anxiety, low (female) fertility

Type O and/or A may be linked to attention-deficit disorder (ADD) in children

Type B may be linked to a lower risk of ADD in children

Type A may be linked to obsessive-compulsive disorder and stomach cancer

Type A, B, and AB may be linked to heart disease and abnormal blood clotting

What can we use from this in teaching undergraduate A&P?

Another interesting aside to throw into an exploration of blood types to "liven up" the conversation a bit to motivate students.

Consider using a diagram of the actual ABO markers to show what's involved at the cellular level—and their similarity to each other.

One may want to mention that blood types may become a factor health professionals may look at when assessing health risks in patients

A classroom discussion on possible mechanisms of a blood-type—health risk could be interesting and useful. This could lead to some great insights about methods of scientific discovery. For example, what's the difference between correlation and cause? How confident should we be in one study?

Consider leading the discussion toward exactly what you want your students to know about blood types and health (e.g., blood donors and recipients, erythroblastosis fetalis, etc.)

Want to know more?

Blood Type Matters for Brain Health

A. Anderson and V. Stern. Scientific American MIND January 1, 2015

Brief article explains discovery that people with AB blood type are at higher risk for age-related cognitive decline. Also lists some of the other blood-type links I mentioned above.

The World Health Organization says it is likely that the virus will spread, as the mosquitoes that carry the virus are found in almost every country in the Americas.

Zika virus was discovered almost 70 years ago, but wasn’t associated with outbreaks until 2007. So how did this formerly obscure virus wind up causing so much trouble in Brazil and other nations in South America?

Where did Zika come from?

Zika virus was first detected in Zika Forest in Uganda in 1947 in a rhesus monkey, and again in 1948 in the mosquito Aedes africanus, which is the forest relative of Aedes aegypti. Aedes aegypti and Aedes albopictus can both spread Zika. Sexual transmission between people has also been reported.

Zika has a lot in common with dengue and chikungunya, another emergent virus. All three originated from West and central Africa and Southeast Asia, but have recently expanded their range to include much of the tropics and subtropics globally. And they are all spread by the same species of mosquitoes.

How did Zika get to the Americas?

Genetic analysis of the virus revealed that the strain in Brazil was most similar to one that had been circulating in the Pacific.

Brazil had been on alert for an introduction of a new virus following the 2014 FIFA World Cup, because the event concentrated people from all over the world. However, no Pacific island nation with Zika transmission had competed at this event, making it less likely to be the source.
There is another theory that Zika virus may have been introduced following an international canoe event held in Rio de Janeiro in August of 2014, which hosted competitors from various Pacific islands.

Another possible route of introduction was overland from Chile, since that country had detected a case of Zika disease in a returning traveler from Easter Island.

Most people with Zika don’t know they have it

According to research after the Yap Island outbreak, the vast majority of people (80 percent) infected with Zika virus will never know it – they do not develop any symptoms at all. A minority who do become ill tend to have fever, rash, joint pains, red eyes, headache and muscle pain lasting up to a week. And no deaths had been reported.

In early 2015, Brazilian public health officials sounded the alert that Zika virus had been detected in patients with fevers in northeast Brazil. Then there was a similar uptick in the number of cases of Guillain-Barré in Brazil and El Salvador. And in late 2015 in Brazil, cases of microcephaly started to emerge.

At present, the link between Zika virus infection and microcephaly isn’t confirmed, but the virus has been found in amniotic fluid and brain tissue of a handful of cases.

The Swiss cheese model for system failure

The Swiss cheese model of accident causation.Davidmack via Wikimedia Commons, CC BY-SA
One way to understand how Zika spread is to use something called the Swiss cheese model. Imagine a stack of Swiss cheese slices. The holes in each slice are a weakness, and throughout the stack, these holes aren’t the same size or the same shape. Problems arise when the holes align.

With any disease outbreak, multiple factors are at play, and each may be necessary but not sufficient on its own to cause it. Applying this model to our mosquito-borne mystery makes it easier to see how many different factors, or layers, coincided to create the current Zika outbreak.

A hole through the layers

The first layer is a fertile environment for mosquitoes. That’s something my colleagues and I have studied in the Amazon rain forest. We found that deforestation followed by agriculture and regrowth of low-lying vegetation provided a much more suitable environment for the malaria mosquito carrier than pristine forest.

Increasing urbanization and poverty create a fertile environment for the mosquitoes that spread dengue by creating ample breeding sites. In addition, climate change may raise the temperature and/or humidity in areas that previously have been below the threshold required for the mosquitoes to thrive.

The second layer is the introduction of the mosquito vector. Aedes aegypti and Aedes albopictus have expanded their geographic range in the past few decades. Urbanization, changing climate, air travel and transportation, and waxing and waning control efforts that are at the mercy of economic and political factors have led to these mosquitoes spreading to new areas and coming back in areas where they had previously been eradicated.

A woman walks away from her apartment as health workers fumigate the Altos del Cerro neighborhood as part of preventive measures against the Zika virus and other mosquito-borne diseases in Soyapango, El Salvador January 21, 2016.

Jose Cabezas/Reuters

For instance, in Latin America, continental mosquito eradication campaigns in the 1950s and 1960s led by the Pan American Health Organization conducted to battle yellow fever dramatically shrunk the range of Aedes aegypti. Following this success, however, interest in maintaining these mosquito control programs waned, and between 1980 and the 2000s the mosquito had made a full comeback.
The third layer, susceptible hosts, is critical as well. For instance, chikungunya virus has a tendency to infect very large portions of a population when it first invades an area. But once it blows through a small island, the virus may vanish because there are very few susceptible hosts remaining.

Since Zika is new to the Americas, there is a large population of susceptible hosts who haven’t previously been exposed. In a large country, Brazil for instance, the virus can continue circulating without running out of susceptible hosts for a long time.

The fourth layer is the introduction of the virus. It can be very difficult to pinpoint exactly when a virus is introduced in a particular setting. However, studies have associated increasing air travel with the spread of certain viruses such as dengue.

When these multiple factors are in alignment, it creates the conditions needed for an outbreak to start.

Putting the layers together

My colleagues and I are studying the role of these “layers” as they relate to the outbreak of yet another mosquito-borne virus, Madariaga virus (formerly known as Central/South American eastern equine encephalitis virus), which has caused numerous cases of encephalitis in the Darien jungle region of Panama.

There, we are examining the association between deforestation, mosquito vector factors, and the susceptibility of migrants compared to indigenous people in the affected area.
In our highly interconnected world which is being subjected to massive ecological change, we can expect ongoing outbreaks of viruses originating in far-flung regions with names we can barely pronounce – yet.

Tuesday, January 5, 2016

When I was an undergraduate—back in the olden days—the first day of every class was always the same. The professor would come in a few minutes after the published start time, hand out a stack of syllabi still fresh with the fumes of the spirit duplicator solvent, and tell us about all the course policies and procedures (anticipating that we would not really read the syllabus). Perhaps there would be a few questions answered. Possibly, we'd get a content-based lecture that first day, but more often we'd just get an early release from class.

When I started teaching college, I did the same thing. I thought that this was how it was supposed to be done. And, despite having had some courses in how to teach effectively, I just fell into the ritual with which I'd grown up.

It didn't even occur to me how boring or pointless this activity was until I was at a HAPS meeting decades ago and went to a workshop entitled something like Engaging Students on the First Day of Class. Although the title was mildly intriguing, the main reason I went was to support my friends Richard Faircloth and Michael Glasgow from Anne Arundel Community College, who presented the workshop. Those of you who've given workshops know that it helps to have a few folks in the crowd who can be counted on to smile back at you even when you're sweating!

It turned out to be one of those many how-did-I-survive-without-knowing-about-this-before-now moments that one experiences at a HAPS Conference. I learned that I could make that first day into something much, much better than the traditional "here's what I expect" sermon.

Richard and Michael had us form small groups and showed us how we could make "syllabus day" a fun, active learning experience for students. An experience that could be far more effective in getting the essential messages across than what I had been doing. It must have worked because I can still see and hear some of what happened nearly two decades ago in my small group—and I took their message home and implemented it.

Their method boils down to this:

Get your students into small groups. Right away—before you've handed out the syllabi or other materials.

Give them a brief handout outlining what they are to do. Or you can project the directions on the screen. For example:

Have them introduce themselves and briefly explain why they are taking A&P.

Have them discuss and write down what pressing questions they have about the course.

Tell them to send someone up to the professor to grab enough syllabi for everyone in the group.

Ask them to use the syllabus and try to find the answers to the questions the group had written down.

It's important NOT to answer their questions as you stroll around to chat and listen in on the groups—they have to find the answers in the syllabus.

Have them re-assemble into a large group and ask them what questions they had that were not answered by their search or that need additional clarification.

By doing this, the students get to know a few other students right away—even the introverts. They get to be active, instead of passively sitting there "absorbing" from an active professor. Students are forced to think about what's important for them to know as they begin a new, perhaps scary-sounding, course. They learn how the syllabus is constructed as they explore it collaboratively looking for critical information. So they know how to find answers to questions they have later in the course. How many times have we wondered if they even looked as the syllabus once?

This method allows the professor to focus their efforts that day on the information that students really want to hear from them at that moment. And it tells you where your syllabus needs to be corrected or clarified!

I was very happy with the way my first experiment with this approach worked. Perhaps more importantly, my students were very happy with it. Ever since that first time, I've regularly had students tell me, "that was fun, I wish all my profs did their first day this way." It even shows up on the end-of-semester course evaluations—so it must have made an impression!

Over the years (nearly twenty), I've tweaked the process and adapted it to my particular course quirks. Because I always get certain questions, I often follow up with a demonstration of how to login to their course in the LMS, how to access the publisher website, and how to register their clickers. I also introduce them to the idea of human science—anatomy and physiology in particular. Ask them to think about why are here—and we discuss those goals and how they can be acheived. I sometimes even give them my secret methods for finding a parking space quickly.

If you'd like a starting point for creating your own first-day experiment, download these example handouts:

About Me

I've worked as an anatomy & physiology professor for several decades, having taught at high school, community college, and university levels. I write A&P textbooks and manuals. I am a President Emeritus of the Human Anatomy and Physiology Society (HAPS) and a founder of HAPS Institute, a continuing education program for A&P professors. I have several blogs and websites related to teaching and learning. And in my youth I was a wild animal trainer.